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去除门静脉淤血减轻肝脏缺血再灌注损伤的实验研究 被引量:3

Experimental study on amelioration of hepatic ischemia reperfusion injury by portal congestion blood removal
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摘要 目的探讨去除门静脉淤血对肝脏缺血再灌注损伤的影响及机制。方法检测家兔肝脏原位冷灌注20、30、40min后淤血的门静脉中内毒素含量变化,观察门静脉淤血去除对恢复灌流后4h血清内毒素、丙氨酸转氨酶(ALT)、透明质酸(HA)、肝组织匀浆丙二醛(MDA)、超氧化物歧化酶(SOD)及肝组织核因子-kB(NF-κB)活性的影响。结果门静脉淤血中内毒素含量随阻断时间延长明显升高(P〈0.01),同一阻断时间每去除2.5ml淤血血清内毒素含量显著下降(P<0.01)。在阻断30min和40min组,去除门静脉淤血能降低血清ALT、HA、及肝组织匀浆MDA的含量和肝组织NF-κB活性,增加肝组织匀浆SOD活性,与不去除相比较差异有统计学意义(P〈0.05)。在阻断20min组去除门静脉淤血与不去除相比较,各检测指标差异无统计学意义(P〉0.05)。结论门静脉淤血中内毒素含量随阻断时间延长明显升高,可能是引起肝脏损伤的主要原因;去除门静脉淤血可以减轻肝脏的再灌注损伤,其机制可能与门静脉淤血去除减少内毒素吸收,进而降低肝组织NF-κB活化有关. Objective To investigate the effect of portal blood stasis removal on hepatic ischemia reperfusion injury and explore its mechanism. Methods A rabbit hepatic model in situ hypothermic irrigation for 20, 30, 40 minutes was established. The endotoxin content in portal blood stasis by an order of 2.5 ml removal was observed. The changes of serum endotoxin, alanine aminotransferase (ALT), hyaluronic acid ( HA), content of malondialdehyde (MDA) and activity of superoxide dismutase (SOD), the activation of nuclear factor-rB (NF-κB) in liver were examined after reperfusion for 4 h. Results The endotoxin content in portal blood stasis was significantly increased by extension of portal vein blocking (P〈0.01). At the same time of portal vein blocking, the endotoxin content significantly decreased with each 2.5 ml blood removal (P〈0. 01). In the group of 30 or 40 minutes portal vein blocking, removing portal blood stasis ameliorated endotoxemia and hepatic ischemia reperfusion injury as shown by serum endotoxin, ALT, HA as well as the amount of MDA, SOD), NF-κB in hepatic tissues (P〈0.05), while the differences were not remarkable in the group of 20 minutes (P〈0. 05). Conclusion The level of serum endotoxin is increased by extension of portal vein blocking and high volume of endotoxin may be responsible for hepatic reperfusion injury. Removing portal blood stasis may protect hepatic ischemia reperfusion injury. The possible mechanism may be that portal blood stasis removal reduced endotoxin absorption to reduce the activation of NF-κB.
出处 《中华肝胆外科杂志》 CAS CSCD 北大核心 2009年第10期764-767,共4页 Chinese Journal of Hepatobiliary Surgery
关键词 再灌注损伤 门静脉淤血 内毒素 核因子-ΚB Reperfusion injury Portal blood stasis Endotoxin Nuclear factor-κB
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  • 1阚彤,杨甲梅,童颖.肝切除术后急性肺损伤和呼吸窘迫综合征的诊治[J].中华肝胆外科杂志,2005,11(2):130-131. 被引量:6
  • 2林胜璋,余耀军,游涛,王飞海,吴伟军,陈聪.大黄素对大鼠肝脏缺血再灌注损伤的预防作用[J].中国中西医结合外科杂志,2006,12(2):136-138. 被引量:16
  • 3彭勇,龚建平,刘长安,李旭宏,刘海忠,李寿柏.大鼠肝移植缺血再灌注后Kupffer细胞CD14基因及蛋白的表达[J].中华肝胆外科杂志,2006,12(4):264-266. 被引量:6
  • 4李洋,刘作金,龚建平.肝缺血-再灌注损伤对大鼠肠黏膜屏障功能及肠道菌群易位的影响[J].中华器官移植杂志,2007,28(3):150-153. 被引量:21
  • 5Li GS, Ye QF, Xia SS, et al. Respiratory distress syndrome after liver transplantation: etiology, prevention and manage ment. Hepatobiliary Pancreat Dis Int, 2002,1:330-334.
  • 6Acosta F, Sabate A. Post-reperfusion syndrome in orthotopic liver transplantation. Rev Esp Anestesiol Reanim, 1996,43: 276- 280.
  • 7Rowlands TE, Homer Vanniasinkam S. Pro-and anti-inflam- matory cytokine release in open versus endovascular repair of abdominal aortic aneurysm. Br J Surg, 2001,88: 1335-1340.
  • 8Sasakawa T, Sasakawa Y, Masunaga T, et al. FK506 sup- presses E selectin, ICAM-1 and VCAM 1 expression on vas- cular endothelial cells by inhibiting tumor necrosis factor alpha secretion from peripheral blood mononuclear cells. Cytokine, 2005,29 : 67-71.
  • 9Pirat A, Ozgur S, Torgay A, et al. Risk factors for postoper- ative respiratory complications in adult liver transplant recipi- ents. Transplant Proc, 2004, 36 : 218- 220.
  • 10Anouk E, Beatrice MG, Frederic D, et al. Proteomic analysis of ischemia-reperfusion injury upon human liver transplanta- tion reveals the protective role of IQGAPI[J]. Mol Cell Pro- teomics, 2006, 5: 1300-1313.

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